Abstract
Shigella flexneri is endemic in most underdeveloped countries, causing diarrheal disease and dysentery among young children. In order to reach its target site, the colon, Shigella must overcome the acid environment of the stomach. Shigella is able to persist in this stressful environment and, because of this ability it can initiate infection following the ingestion of very small inocula. Thus, acid resistance is considered an important virulence trait of this bacterium. It has been reported that moderate acid conditions regulate the expression of numerous components of the bacterial envelope. Because the lipopolysaccharide (LPS) is the major component of the bacterial surface, here we have addressed the role of LPS in acid resistance of S. flexneri 2a. Defined deletion mutants in genes encoding proteins involved in the synthesis, assembly and length regulation of the LPS O antigen were constructed and assayed for resistance to pH 2.5 after adaptation to pH 5.5. The results showed that a mutant lacking O antigen was significantly more sensitive to extreme acid conditions than the wild type. Not only the presence of polymerized O antigen, but also a particular polymer length (S-OAg) was required for acid resistance. Glucosylation of the O antigen also contributed to this property. In addition, a moderate acidic pH induced changes in the composition of the lipid A domain of LPS. The main modification was the addition of phosphoethanolamine to the 1′ phosphate of lipid A. This modification increased resistance of S. flexneri to extreme acid conditions, provide that O antigen was produced. Overall, the results of this work point out to an important role of LPS in resistance of Shigella flexneri to acid stress.
Highlights
Species of the genus Shigella are the cause of shigellosis, a diarrheal disease that is endemic in developing countries [1]
We investigated whether the lipopolysaccharide of S. flexneri 2a is modified by exposure to a moderate acidic pH, and if these modifications increase bacterial resistance to extreme acidity
Our results clearly show that the presence of O antigen (OAg) is required for acid resistance, since a mutant that does not bind the polymer to the lipid A-core was highly sensitive to pH 2.5, even after being adapted to pH 5.5
Summary
Species of the genus Shigella are the cause of shigellosis, a diarrheal disease that is endemic in developing countries [1]. In contrast to other bacterial enteric pathogens, such as Vibrio cholerae or Salmonella Typhi, species of Shigella are able to initiate infection of humans following ingestion of 10 to 100 bacteria, without neutralization of gastric acid [3,4,5]. For this reason, acid survival is considered an important pathogenic characteristic of these species [4]. The acid-resistance pathway 1, or oxidative system, is similar to that of Escherichia coli and requires complex media, oxidative growth and acid induction. A third system, which is induced in minimal media under fermentative conditions, has been described in S. flexneri 2457T [8]
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